scholarly journals Pigment-epithelium-derived factor (PEDF) occurs at a physiologically relevant concentration in human blood: purification and characterization

2003 ◽  
Vol 374 (1) ◽  
pp. 199-206 ◽  
Author(s):  
Steen V. PETERSEN ◽  
Zuzana VALNICKOVA ◽  
Jan J. ENGHILD
Keyword(s):  
Pigment Epithelium ◽  
Protein A ◽  
Physiological Role ◽  
The Body ◽  
Systemic Delivery ◽  
Blocking Group ◽  
Post Translational Modifications ◽  
Pigment Epithelium Derived Factor ◽  
Vessel Growth

Pigment epithelium-derived factor (PEDF) inhibits the formation of blood vessels in the eye by inducing apotosis in actively dividing endothelial cells. The activity of PEDF equals or supersedes that of other anti-angiogenic factors, including angiostatin, endostatin and thrombospondin-1. In addition, PEDF has the potential to promote the survival of neurons and affect their differentiation. Here we show that PEDF is present in plasma at a concentration of approx. 100 nM (5 μg/ml) or twice the level required to inhibit aberrant blood-vessel growth in the eye. Thus the systemic delivery of PEDF has the potential to affect angiogenesis or neurotrophic processes throughout the body, significantly expanding the putative physiological role of the protein. A complete map of all post-translational modifications revealed that authentic plasma PEDF carries an N-terminal pyroglutamate blocking group and an N-linked glycan at position Asn266. The pyroglutamate residue may regulate the activity of PEDF analogously to the manner in which it regulates thyrotropin-releasing hormone.

Role of pigment epithelium-derived factor (PEDF) on arsenic-induced neuronal apoptosis

Chemosphere ◽  
2019 ◽  
Vol 215 ◽  
pp. 925-931 ◽  
Author(s):  
Wei Zhang ◽  
Xiaohui Cui ◽  
Yanhui Gao ◽  
Liyan Sun ◽  
Jing Wang ◽  
...  
Keyword(s):  
Neuronal Apoptosis ◽  
Pigment Epithelium ◽  
Pigment Epithelium Derived Factor

Role of Pigment Epithelium-Derived Factor (PEDF) in Photoreceptor Cell Protection

2001 ◽  
pp. 119-126
Author(s):  
Wei Cao ◽  
Joyce Tombran-Tink ◽  
Rajesh Elias ◽  
Steven Sezate ◽  
James F. McGinnis
Keyword(s):  
Photoreceptor Cell ◽  
Pigment Epithelium ◽  
Cell Protection ◽  
Pigment Epithelium Derived Factor

scholarly journals Store-Operated Calcium Channels in Physiological and Pathological States of the Nervous System

2020 ◽  
Vol 14 ◽  
Author(s):  
Isis Zhang ◽  
Huijuan Hu
Keyword(s):  
Nervous System ◽  
Calcium Channels ◽  
Neurological Disorders ◽  
Neurological Diseases ◽  
Physiological Role ◽  
The Body ◽  
Store Operated Calcium Entry ◽  
Important Pathway ◽  
Molecular Components

Store-operated calcium channels (SOCs) are widely expressed in excitatory and non-excitatory cells where they mediate significant store-operated calcium entry (SOCE), an important pathway for calcium signaling throughout the body. While the activity of SOCs has been well studied in non-excitable cells, attention has turned to their role in neurons and glia in recent years. In particular, the role of SOCs in the nervous system has been extensively investigated, with links to their dysregulation found in a wide variety of neurological diseases from Alzheimer’s disease (AD) to pain. In this review, we provide an overview of their molecular components, expression, and physiological role in the nervous system and describe how the dysregulation of those roles could potentially lead to various neurological disorders. Although further studies are still needed to understand how SOCs are activated under physiological conditions and how they are linked to pathological states, growing evidence indicates that SOCs are important players in neurological disorders and could be potential new targets for therapies. While the role of SOCE in the nervous system continues to be multifaceted and controversial, the study of SOCs provides a potentially fruitful avenue into better understanding the nervous system and its pathologies.

scholarly journals The Role of the Endothelin System in the Vascular Dysregulation Involved in Retinitis Pigmentosa

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Francesco Saverio Sorrentino ◽  
Claudio Bonifazzi ◽  
Paolo Perri
Keyword(s):  
Blood Flow ◽  
Retinitis Pigmentosa ◽  
Vascular System ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Ocular Blood Flow ◽  
The Body ◽  
Vascular Dysregulation ◽  
Endothelin System

Retinitis pigmentosa is a clinical and genetic group of inherited retinal disorders characterized by alterations of photoreceptors and retinal pigment epithelium leading to a progressive concentric visual field restriction, which may bring about severe central vision impairment. Haemodynamic studies in patients with retinitis pigmentosa have demonstrated ocular blood flow abnormalities both in retina-choroidal and in retroocular vascular system. Moreover, several investigations have studied the augmentation of endothelin-1 plasma levels systemically in the body and locally in the eye. This might account for vasoconstriction and ischemia, typical in vascular dysregulation syndrome, which can be considered an important factor of reduction of the ocular blood flow in subjects affected by retinitis pigmentosa.

scholarly journals Emerging concepts regarding pannexin 1 in the vasculature

2015 ◽  
Vol 43 (3) ◽  
pp. 495-501 ◽  
Author(s):  
Miranda E. Good ◽  
Daniela Begandt ◽  
Leon J. DeLalio ◽  
Alexander S. Keller ◽  
Marie Billaud ◽  
...  
Keyword(s):  
Vascular Function ◽  
Atp Release ◽  
The Body ◽  
Purinergic Signalling ◽  
Molecular Tools ◽  
Cellular Functions ◽  
Post Translational Modifications ◽  
Pannexin 1 ◽  
Knockout Animals

Pannexin channels are newly discovered ATP release channels expressed throughout the body. Pannexin 1 (Panx1) channels have become of great interest as they appear to participate in a multitude of signalling cascades, including regulation of vascular function. Although numerous Panx1 pharmacological inhibitors have been discovered, these inhibitors are not specific for Panx1 and have additional effects on other proteins. Therefore, molecular tools, such as RNA interference and knockout animals, are needed to demonstrate the role of pannexins in various cellular functions. This review focuses on the known roles of Panx1 related to purinergic signalling in the vasculature focusing on post-translational modifications and channel gating mechanisms that may participate in the regulated release of ATP.

scholarly journals Physiology and clinical importance of the natriuretic peptide system

2011 ◽  
Vol 152 (26) ◽  
pp. 1025-1034
Author(s):  
Gábor Szabó ◽  
János Rigó jr. ◽  
Bálint Nagy
Keyword(s):  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Physiological Role ◽  
Clinical Importance ◽  
The Body ◽  
Diagnosis And Prognosis ◽  
Peptide Family ◽  
Peptide System ◽  
Pressure Changes

In the last three decades many members of the natriuretic peptide family was isolated. The function and physiological role of these peptides are pleiotropic. All natriuretic peptides are synthesized from polypeptide precursors. Together with the sympathetic nervous system and other hormones they play key roles, like an endogenous system in the regulation of the body fluid homeostasis and blood pressure. Changes in this balance lead to dysfunction in the endothel and left ventricle, which can cause severe complications. In many cardiovascular diseases natriuretic peptides serve not only as marker for diagnosis and prognosis but they have therapeutic importance. In the last years the potential use of the elevated BNP levels for diagnosis of pre-eclampsia was examined. In our review we discuss the current understanding of molecular biology, biochemistry and clinical relevance of natriuretic peptides. Orv. Hetil., 2011, 152, 1025–1034.

scholarly journals RIPK1-Associated Inborn Errors of Innate Immunity

2021 ◽  
Vol 12 ◽  
Author(s):  
Jiahui Zhang ◽  
Taijie Jin ◽  
Ivona Aksentijevich ◽  
Qing Zhou
Keyword(s):  
Immune Deficiency ◽  
Molecular Mechanisms ◽  
Clinical Manifestations ◽  
Physiological Role ◽  
Model Organisms ◽  
Loss Of Function ◽  
Inborn Errors ◽  
Post Translational Modifications ◽  
Cell Death Signaling

RIPK1 (receptor-interacting serine/threonine-protein kinase 1) is a key molecule for mediating apoptosis, necroptosis, and inflammatory pathways downstream of death receptors (DRs) and pattern recognition receptors (PRRs). RIPK1 functions are regulated by multiple post-translational modifications (PTMs), including ubiquitination, phosphorylation, and the caspase-8-mediated cleavage. Dysregulation of these modifications leads to an immune deficiency or a hyperinflammatory disease in humans. Over the last decades, numerous studies on the RIPK1 function in model organisms have provided insights into the molecular mechanisms of RIPK1 role in the maintenance of immune homeostasis. However, the physiological role of RIPK1 in the regulation of cell survival and cell death signaling in humans remained elusive. Recently, RIPK1 loss-of-function (LoF) mutations and cleavage-deficient mutations have been identified in humans. This review discusses the molecular pathogenesis of RIPK1-deficiency and cleavage-resistant RIPK1 induced autoinflammatory (CRIA) disorders and summarizes the clinical manifestations of respective diseases to help with the identification of new patients.

Protective role of pigment epithelium-derived factor (PEDF) in early phase of experimental diabetic retinopathy

2009 ◽  
Vol 25 (7) ◽  
pp. 678-686 ◽  
Author(s):  
Yumiko Yoshida ◽  
Sho-Ichi Yamagishi ◽  
Takanori Matsui ◽  
Yuko Jinnouchi ◽  
Kei Fukami ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Early Phase ◽  
Pigment Epithelium ◽  
Protective Role ◽  
Pigment Epithelium Derived Factor

About early diagnosis of vitamin deficiency

1937 ◽  
Vol 33 (2) ◽  
pp. 121-126
Author(s):  
E. M. Lepsky
Keyword(s):  
Vitamin A ◽  
Clinical Symptoms ◽  
Vitamin A Deficiency ◽  
Physiological Role ◽  
Vitamin Deficiency ◽  
The Body ◽  
Vitamin Deficiencies ◽  
Complete Diet ◽  
Digestive Disorders

In the expressed form of avitaminosis, we are now observed less and less. Nevertheless, the problem of vitamin deficiencies remains relevant for the practitioner. As the physiological role of vitamins and their importance in pathology becomes more and more clear, the presence of light, "erased" forms, which are more correctly called hypovitaminosis, becomes more and more obvious. Experience shows that the generally accepted ideas about the conditions for the occurrence of avitaminosis should be revised. Not only in the absence or in the absence of one or another vitamin in food, vitamin deficiency can develop. More and more observations are accumulating showing that a weak or even strongly pronounced vitamin deficiency can appear in a person who receives a completely complete diet. This phenomenon, paradoxical at first glance, can take place under the following circumstances: with digestive disorders associated with impaired absorption; with liver diseases (the latter is especially important for vitamin A deficiency, since the conversion of carotene into vitamin A suffers); when the need for vitamins is increased against the norm, for example, in rapidly growing children or in lactating women who excrete significant amounts of vitamin C with milk; with increased destruction of vitamin stores in the body, which is observed with all kinds of infections and other febrile and debilitating diseases. To what has been said, it must also be added that very often our food turns out to be poor in vitamins, due to irrational preparation, improper storage of food, peculiar deviations of appetite, etc. In the earliest stages, when even mild clinical symptoms do not yet exist, modern methods of studying vitamins can the presence of latent hypovitaminosis. This is especially evident in the example of the scourge.

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